# Health Protection Agency

Compendium of Chemical Hazards:

Diesel.

Prepared by:



## Robert P Chilcott

Chemical Hazards and Poisons Division (HQ), Chilton, Didcot, Oxfordshire, OX11 0RQ, United Kingdom.

www.hpa.org.uk

Disclaimer



### This guidance has been provided by the Chemical Hazards and Poisons

Division of the UK Health Protection Agency (HPA). It is general guidance based on current knowledge and unders tanding. The HPA does not warrant that the information and guidance is complete and correct for use in all

circumstances. The HPA shall not be lia ble for any damages that might be

incurred as a result of the use of the guidance or information.

# HPA Compendium of Chemical Hazards

Diesel

Key Points

Fire

• Flammable

• Vapour / air mixtures may be explosive

• Use foam and liquid-tight protective clothing with breathing apparatus



### Health

• Irritating to eyes, respiratory ststem and skin

• Severe lung injury may occur following aspiration of liquid

• Possible carcinogen



### Environment

• Dangerous for the environment

• Inform Environment Agency of substantial incidents



### Prepared by R P Chilcott,
CHAPD HQ

2006

Version 1DIESEL – CONTENTS



## Contents

GENERAL INFORMATION

Background

Production and Uses

Frequently Asked Questions



### INCIDENT MANAGEMENT

Hazard Identification

Standard (UK) Dangerous Goods Emergency Action Codes Chemical Hazard Information and Packaging for Supply Classification ()

Physicochemical Properties

Threshold Toxicity Values

Published Emergency Response Guidelines

Emergency Response Planning Guideline (ERPG) Values Acute Exposure Guideline Levels (AEGLs)

Exposure Standards, Guidelines or Regulations

Occupational standards Public health guidelines

Health Effects

Major route of exposure Immediate Signs or Symptoms of Acute Exposure

Decontamination and First Aid

Dermal exposure Ocular exposure

Inhalation Ingestion



### TOXICOLOGICAL OVERVIEW

Toxicological Overview

Summary of health effects

Kinetics and metabolism Sources and route of human exposure

Health Effects of Acute / Single Exposure

Human Data General toxicity

Inhalation Ingestion Dermal / ocular exposure Neurotoxicity Nephrotoxicity Delayed effects following an acute exposure

Animal and In-Vitro DataGeneral toxicity Delayed effects following an acute exposure

Health Effects of Chronic / Repeated Exposure

Human Data General toxicity

Inhalation Ingestion Dermal / ocular exposure Genotoxicity Carcinogenicity Reproductive and developmental toxicity

Animal and In-Vitro Data General toxicity

Inhalation Ingestion Dermal / ocular exposure Genotoxicity Carcinogenicity Reproductive and developmental toxicity

References

Annex I: Categories of diesel additives.

Annex II: UK Classification of fuel oils.

Annex III: UK Physicochemical standards for diesel

# Diesel

General information

Key Points

Fire

• Flammable

• Vapour / air mixtures may be explosive

• Use foam and liquid-tight protective clothing with breathing apparatus



### Health

• Irritating to eyes, respiratory system and skin

• Chemical pneumonitis may arise following aspiration of vomitus (secondary to ingestion) or inhalation of aerosol (or aspiration of liquid) during manual siphoning

• Prolonged skin exposure may cause skin irritation

• Possible carcinogen

• Diesel is considered not to be a human reproductive or developmental toxicant



### Environment

• Dangerous for the environment

• Inform Environment Agency of substantial incidents



### Prepared by R P Chilcott,
CHAPD HQ

2006

Version 1DIESEL – GENERAL INFORMATION



## Background

Diesel is a complex mixture of chemicals mainly obtained from the distillation of crude oil. The product is thought to be named after Dr Rudolf Diesel, a German engineer who, in 1892, patented an oil-burning internal combustion engine. Modern diesel engines also incorporate features of a design (patented between 1886 and 1890) by the Yorkshireman Herbert Akroyd Stuart .

In the UK, ‘diesel’ or DERV refers to a fuel for running cars, vans and lorries. However,

the term ‘diesel’ is also used to describe a range of different fuels such as ‘artic’ and

‘marine’ diesel or as an alternative name for kerosene, all of which differ considerably in composition and physical properties.

In 2004, approximately 700 litres (150 gallons) of diesel was sold every second in the UK. Most diesel is ultra-low in sulphur

content in order to limit the emission of sulphur-containing pollutants from engine

exhaust fumes.

Diesel is not considered to be particularly toxic and accidental poisoning is very rare. However, if diesel is swallowed, medical advice should be obtained immediately as there is a small risk of short-term lung damage if vomiting occurs or if droplets of diesel are inhaled. Long-term skin exposure to diesel may result in eczema (dermatitis)

and should be avoided. The use of diesel to clean skin and hair should be strongly discouraged as this practice has been known to cause serious kidney damage.DIESEL – GENERAL INFORMATION



## Production and Uses

Key Points

Production and uses

• Diesel is produced by mixing fractions of crude oil distillates (petrochemicals) with various, brand-specific additives.

• Approximately 22 thousand million litres (5 thousand million gallons) of diesel were sold in the UK in 2004, equating to 700 litres (150 gallons) per second.

Diesel is produced by blending straight-run middl e distillates (minimum 40%) with varying proportions of straight-run gas oil, light vacuum distillates, light thermally-cracked distillates and light catalytically-cracked distillates.

The quantity of diesel released by HM Revenue and Customs for consumption in the UK in 2004 was approximately 22 thousand million litres (5 thousand million gallons), the majority (99.7%) of which was “ultra-low sulphur diesel” for automotive engines. Diesel is also used as a cleaning solvent for tanks, engines and refinery equipment.DIESEL – GENERAL INFORMATION



## Frequently Asked Questions

What is diesel?

Diesel is a complex mixture of hydrocarbons produced by mixing fractions obtained from the distillation of crude oil with brand-specific addit ives to improve performance. It is a liquid

under normal conditions with a characteristic odour.



### What is diesel used for?

In the UK, diesel is mainly used as a fuel for road vehicles, although other forms of transport (such as ships and trains) and electricity generators also use certain types of diesel.



### How does diesel get into the environment?

Diesel is found in the environment as a result of accidental release from an industrial site or transport vehicle. There are no natural sources of diesel.



### If there is diesel in the environment will I have any adverse health effects?

Like most chemicals, the amount of diesel you are exposed to must be above a certain level to cause adverse health effects. A short, one- off exposure to diesel will not normally cause any long-term health effects. Occasional skin exposure may lead to dermatitis (eczema).Breathing large quantities of diesel vapour or drinking diesel-based fluids may cause nonspecific signs and symptoms of poisoning such as dizziness, headache and vomiting. A severe form of lung damage called pneumonitis may occur if liquid diesel is inhaled directly onto the lungs, for example, whilst manually siphoning a tank or from inhaling vomit after swallowing diesel. This is why it is important not to make someone sick if they have

swallowed diesel.



### Can diesel cause cancer?

There is limited evidence from animal studies that prolonged exposure may increase the risk of developing skin cancer. There is not thought to be any risk of cancer from short-term, occasional exposure.



### Can diesel affect or damage the unborn child?

There is no evidence to suggest that exposure of a mother to diesel may harm the unborn child. However, as with all chemicals, it is obviously best to avoid unnecessary contact if possible.

# Diesel

Incident management

Key Points

Fire

• Flammable

• Vapours may be violently reactive with air

• Use foam and liquid-tight protective clothing with breathing apparatus



### Health

• Toxicity occurs following ingestion, inhalation & skin absorption

• Possible carcinogen

• Irritating to eyes and skin

• Aspiration may cause serious lung injury



### Environment

• Avoid release into the environment

• Inform Environment Agency of substantial incidents



### Prepared by R P Chilcott,
CHAPD HQ

2006

Version 1DIESEL – INCIDENT MANAGEMENT



## Hazard Identification ( ) a



### Standard (UK) Dangerous G oods Emergency Action Codes

UN 1202 Diesel Fuel or Gas Oil or Heating Oil, Light

EAC 3Y Use normal foam. Wear normal fire kit in combination with breathing apparatus * . Spillages and decontamination run-off should be prevented from entering drains and watercourses. Substance can be violently or explosively reactive.

APP -

Class 3 Flammable liquid

Hazards

Sub

risks -

HIN 30 Flammable liquid (flash point between 23 °C and 61 °C inclusive) or flammable liquid or solid in the molten state with a flash point above 61 °C, heated to a temperature equal to or above its flash point, or self-heating liquid UN – United Nations number; EAC – Emergenc y Action Code; APP – Additional Personal Protection; HIN - Hazard Identification Number

* Normal fire fighting clothing i.e. fire kit (BS EN 469), gloves (BS EN 659) and boots (HO specification A29 and A30) in combination with self-contain ed open circuit positive pressure compressed air breathing apparatus (BS EN 137).

a Dangerous goods emergency action code list, HM Fire Service Inspectorate, Publications Section, The Stationery Office, 2004.DIESEL – INCIDENT MANAGEMENT



### Chemical Hazard Information and Packaging for Supply Classification ( ) a

Classification Carc cat 3 Category 3 carcinogen

Risk phrases R40 Limited evidence of a carcinogenic effect

S(2) Keep out of the reach of children Safety phrases S36/37 Wear suitable protective clothes and gloves

a Approved supply list (seventh edition): informat ion approved for the classification and labelling of substances and preparations dangerous for supply. Chemical (Hazard Information and Packaging for Supply) Regulations 2002. The Stationery Office, 2002.

## Physicochemical Properties ( , ) a b

Volatility Low volatility; vapour pressure < 1 mm Hg

Specific gravity 0.82 – 0.95 at 15 °C (water = 1)

Flammability Flammable.

Lower explosive limit 0.6%

Upper explosive limit 6.5%

Water solubility 0.5 mg 100 mL -1

Reactivity Vapours may be violently reactive with air

Reaction or degradation products May liberate irritating or toxic fumes during combustion

Odour Characteristic odour DIESEL – INCIDENT MANAGEMENT

a International Chemical Safety Card (ICSC) entry for diesel fuel no 2. ISCS 1561. International Occupational Safety and Health Information Centre (CIS), 2004.

b CIRUS entry for diesel, 2005.DIESEL – INCIDENT MANAGEMENT



## Threshold Toxicity Values ( ) a



## THRESHOLD LEVELS

EXPOSURE BY INHALATION

ppm mg m -3 SYMPTOMS

- - Data not available

a Hydrocarbons (MEDITEXT® Medical Management). In: Klasco RK (Ed): TOMES® System. Thomson Micromedex, Greenwood Village, Co lorado (Edition expires [03, 2006]).DIESEL – INCIDENT MANAGEMENT



## Published Emergency Response Guidelines

Emergency Response Planning Guideline (ERPG) Values ( ) a

Listed value (ppm) Calculated value (mg m -3 )

ERPG-1 *

ERPG-2 *

ERPG-3 * Data not available

* Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing other than mild transient adverse health effects or perceiving a clearly defined, objectionable odour.

** Maximum airborne concentration below which it is believed that nearly all individuals could be exposed for up to 1 hr without experiencing or developing irreversible or other serious health effects or symptoms which could impair an individual's ability to take protective action.

*** Maximum airborne concentration below wh ich it is believed that nearly allindividuals could be exposed for up to 1 hr without experiencing or developing lifethreatening health effects.



### Acute Exposure Guideline Levels (AEGLs) ( ) b

mg m -3

10 min 30 min 60 min 4 hr 8 hr

AEGL-1 †

AEGL-2 ††

AEGL-3 ††† Data not available

† The level of the chemical in air at or above which the general population could experience notable

discomfort.

†† The level of the chemical in air at or above which there may be irreversible or other serious longlasting effects or impaired ability to escape.

††† The level of the chemical in air at or above which the general populati on could experience lifethreatening health effects or death.

a American Industrial Hygiene Association (AIHA). Emergency Response Planning Guideline values and Workplace Environmental Exposure Level Guides Handbook, Fairfax, VA, 2005.

b U.S. Environmental Protection Agency.DIESEL – INCIDENT MANAGEMENT



## Exposure Standards, Guidelines or Regulations

Occupational standards

LTEL(8 hour reference period): No guideline value specified

WEL
STEL(15 min reference period): No guideline value specified



### Public health guidelines

DRINKING
WATER QUALITY GUIDELINE No guideline value specified

AIR QUALITY GUIDELINE No guideline value specified

SOIL GUIDELINE VALUE AND
HEALTH CRITERIA VALUES No guideline values specified

WEL – Workplace exposure limit; LTEL - Long- term exposure limit; STEL – Short-term exposure limitDIESEL – INCIDENT MANAGEMENT



## Health Effects ( ) a



### Major route of exposure

• Toxicity may occur following ingestion, inhalation or skin exposure.



### Immediate Signs or Symp toms of Acute Exposure (b-d) ( , , ) b c d

• Inhalation: May cause headache, dizziness, drowsiness, incoordination and euphoria. Aspiration into the lungs causes pneumonitis with choking, coughing, wheeze, breathlessness, cyanosis and fever.

• Ingestion: Often no symptoms occur but there may be nausea, vomiting and occasionally diarrhoea.

• Ocular exposure: This product is expected to be pH neutral but may be irritating to the eyes causing an immediate stinging and burning sensation with lachrymation.

• Dermal exposure: Irritant. Drying and cracking due to defatting action. There may be transient pain with erythema, blistering and superficial burns.

For more information see TOXBASE (http://www.spib.axl.co.uk)

a TOXBASE: Diesel oil, 2002.

b TOXBASE: Petroleum distillates – features and management, 2002.

c TOXBASE: Eye irritants, 2002.

d TOXBASE: Skin decontami nation – irritants, 1996.DIESEL – INCIDENT MANAGEMENT



## Decontamination and First Aid ( , ) a b

Important Notes

• Many patients remain well and need no treatment.

• Ambulance staff, paramedics and emergency department staff treating chemicallycontaminated casualties should be equipped with NHS approved liquid-tight PPE and blow-over respirators with a A2B2EK filter, where appropriate.



### Dermal exposure ( ) c

• Remove patient from exposure.

• Remove all soiled clothing.

• Wash the contaminated area thoroughly with soap and water.

• Treat symptomatically.



### Ocular exposure ( ) d

• Remove patient from exposure.

• Remove contact lenses if necessary and immediately irrigate the affected eye thoroughly with water or 0.9% saline for at least 10-15 minutes.



### Inhalation ( ) e

• Remove patient from exposure and give oxygen.

• Maintain a clear airway and adequate ventilation.

• Apply other measures as indicated by the patient’s clinical condition.



### Ingestion (e)

• Gastric lavage should not be undertaken. Consider gastric aspiration within 1 hour of ingestion, if very large amounts have been undertaken, provided the airway can be protected.

• Give oxygen if symptomatic.

• Patients who have ingested small amounts and have had no symptoms suggestive of aspiration (choking, coughing, vomiting) or other features since the exposure can be observed at home under supervision for 6 hours after ingestion, with advice to attend hospital if features develop.

• Patients who have had features of possible aspiration should be referred to hospital.

• Patients with persistent respiratory symptoms, drowsiness or convulsions should be admitted to hospital.

a Decontamination and chemical personal protective equipment in the National Health Service: Current provision, consensus opinion, specification and training implications. A report on progress. The National Focus on Chemical Incidents, 2001.

b TOXBASE: Diesel oil, 2002.

c TOXBASE: Skin decontami nation – irritants, 1996.

d TOXBASE: Eye irritants, 2002.

e TOXBASE: Petroleum distillates – features and management, 2002. TOXBASE - http://www.spib.axl.co.uk

# Diesel

Toxicological overview

Key Points

Kinetics and metabolism

• As diesel is a mixture of chemicals, there is no definitive ADME (absorption, distribution, metabolism and excretion) data



### Health effects of acute exposure

• Diesel may be irritating to the eyes, respiratory system and skin

• The main hazard associated with diesel is chemical pneumonitis that may arise following aspiration of vomitus (secondary to ingestion) or inhalation of aerosol (or aspiration of liquid) during manual siphoning



### Health effects of chronic exposure

• Prolonged skin exposure to diesel may cause a variety of dermatitic conditions and is generally a result of inadequate or inappropriate use of personal protective equipment

• Diesel does not have a measurable effect on human reproduction or development

• There is currently no unequivocal evidence to link diesel with the incidence of cancer in humans but there is limited evidence for carcinogenicity in animals following prolonged exposure



### Prepared by R P Chilcott,
CHAPD HQ

2006

Version 1DIESEL – TOXICOLOGICAL OVERVIEW



## Toxicological Overview

Diesel is a complex mixture of hydrocarbons produced by blending several fractions of crude oil distillates with brand-specific chemical additives a (Annex I) [1]. The actual chemical composition of diesel varies widely according to the geographical source of crude oil, but generally comprises C 8 – C 21 aliphatic hydrocarbons (boiling range 160 – 360 oC) with up to 25% aromatic compounds.

The (UK) technical terms for diesel are “Class A1 Fuel Oil” and “Class A2 Fuel Oil” and refer to use in domestic and agricultural vehicles, respectively (Annex II). For the purpose of this document, “diesel” will be used as a synonym for A1 fuel oil.

Given its complex and highly variable composition, diesel is defined by physical characteristics rather than by c hemical constituents (Annex III) [2].

This note does not consider diesel fumes ar ising from use in vehicle engines or from

uncontrolled combustion.

a Diesel may also contain dyes or markers and up to 5% fatty acid methyl esters (FAME) in compliance with EN 14214:2003. Examples of additives are given at Annex I.DIESEL – TOXICOLOGICAL OVERVIEW



### Summary of health effects

The principal adverse effect arising from the ingestion of diesel is chemical pneumonitis (secondary to aspiration of vomitus) [3, 4].

There is limited evidence to suggest that diesel may be nephrotoxic [5, 6].

Ingestion of diesel or acute exposure to vapour may lead to general signs of intoxication such as mild CNS symptoms (dizziness, headache, nausea) and vomiting [7, 8].

Skin exposure to diesel may result in dermatitis [3, 7].

Certain types of diesel are non-genotoxic animal carcinogens and are classified as Category 3 carcinogens under CHIP [8, 9].DIESEL – TOXICOLOGICAL OVERVIEW



### Kinetics and metabolism

As diesel is a mixture of chemicals, there is no definitive ADME data available for either animals or humans [9]. The onset of local or systemic effects following dermal, oral or pulmonary exposure indicates that these are all potential routes of absorption for diesel.



### Sources and route of human exposure

Occupational exposure may potentially occur during manual filling or discharge operations within the petrochemical industry [10], repair or service of diesel engines or from practices where diesel is used as a cleaning agent or solvent [9].

Domestic exposure to diesel is uncommon, although limited skin exposure may occur whilst refuelling domestic vehicles and pulmonary exposure may result from aspiration of liquid during manual siphoning. Leakage of diesel onto hot engine manifolds may liberate a respirable aerosol of micrometer-sized diesel particles [11].

Large-scale environmental contamination has occu rred following the release of diesel from storage tanks and sea tankers [9] and some conc ern has been expressed over health effects of vapour arising from contaminated soil [12].

Diesel accounted for all spillages resulting from road traffic incidents in the UK during 2003 and 42% of all significant 18 (Environment Agency Category 1 or 2) pollution incidents for the same period [13].

18 Significant refers to a Category 1 or 2 incident as defined by the Environment Agency’s National Incident Recording System (Common Incident Classification, or CIC).DIESEL – TOXICOLOGICAL OVERVIEW



## Health Effects of Acute / Single Exposure

Human Data

General toxicity

Under normal conditions of storage, handling or use as fuel, diesel should not present a hazard to health providing excessive skin contact is avoided [14]. The main hazard associated with diesel is chemical pneumonitis t hat may arise following aspiration of vomitus (secondary to ingestion) or inhalation of aerosol (or aspiration of liquid) during manual siphoning [4, 8].

There are few studies investigating the toxicity of diesel per se . Therefore, toxicological evaluations of diesel tend to be derived by consi dering the toxicity of similar (middle distillate) products such as kerosene and petrol [4, 8, 9, 11]. However, such comparisons do not take into account the toxicity of brand-specific additives, the effects of which cannot be predicted from complex hydrocarbon mixtures. Therefore, this note will mainly consider studies that are specific to diesel.

Inhalation

One study has examined the effects of a co mbined exposure to diesel (5 ppm) and acetaldehyde (0.5 ppm) in Gulf War veterans but did not report any adverse effects in healthy volunteers [15].

It has been stated that inhalation of diesel vapour may lead to CNS / respiratory depression and cardiac arrhythmias [7]. There do not, however, appear to be any specific case studies to confirm these effects; it is assumed that the (limited) presence of low molecular weight hydrocarbons in diesel is sufficient to contribute to such signs of toxicity [16]. Most clinical instances of myocardial sensitisation occur fo llowing exposure to volatile solvents such as those found in adhesives, lighter fluid, nail polish remover and aerosol propellants [17]. Diesel vapour (at 37°C) predominantly contains C 10+ hydrocarbons [18].

Direct aspiration of diesel [19] or aspiration of contaminated vomit is a secondary source of pulmonary exposure that may lead to chemical (lipoidal) pneumonitis [20], a delayed onset and potentially fatal lung disorder characterised by cyanosis, dyspnoea and chest x-ray opacities [21].

Ingestion

The signs of toxicity following oral intake are generally stated to include nausea, vomiting, diarrhoea, irritation of the aero-digestive and GI tracts [7]. In one reported case of intentional self-poisoning, chemical pneumonitis was observed (which may have been due to aspiration of vomitus) [22].DIESEL – TOXICOLOGICAL OVERVIEW

Dermal / ocular exposure

Eye exposure to diesel may cause transient pain and/or hyperaemia [7]. Diesel is generally considered to be less irritating to the eyes than other middle distillate fuels such as kerosene or petrol [8].

Acute dermal exposure may result in local irritation (erythema, pruritis) which is generally more severe than that seen with other middle distillate products [23]. The incorporation of additives (such as biocides) may augment dermal sensitivity to diesel [24]. It has been suggested that the inclusion of visible markers (dyes) may increase the self-perceived dermal irritancy of diesel [25].

Neurotoxicity

No reports on the neurological effects of human diesel exposure were available in the literature. However, diesel is known to contain a number of potentially neurotoxic substances [11] and exposure to other mid-distillate fuels has resulted in neurological disorders including drowsiness, neurasthenia and decreased sensorimotor speed [4].

Nephrotoxicity

Several case studies have cited acute renal failure (secondary to acute renal tubular necrosis) as a potential complication following acute exposure to diesel [6, 8, 9, 26]. Signs included oliguria (progressing to anuria), nausea, abdominal cramps and diarrhoea.

Delayed effects following an acute exposure

There is limited evidence to suggest that long-term pulmonary residua may occur following chemical pneumonitis (as a result of aspirati on-induced pneumonitis) [20, 27]: these chronic effects are of unknown clinical relevance [28].



### Animal and In-Vitro Data

General toxicity

The oral toxicity of diesel is relatively low, with two studies reporting LD 50 values of 7.5 g kg -1
[29] and 16 ml kg -1 in the rat 19 [30]. Diesel was reported as being non-irritating to the eyes but severely irritating to skin of rabbits [29]. No deaths were reported following acute dermal exposure to 5 g kg -1 in rats [9].

In a study using rats, a Ct of 1440 mg min m -3 was not lethal if given as a 4 hour exposure, but the same Ct was lethal for a 6 hour exposure [4].

19 Conversion from ml kg -1 to g kg -1 was not possible, as the density of the material used in the study

was not stated.DIESEL – TOXICOLOGICAL OVERVIEW

Delayed effects following an acute exposure

The available literature pertaining to the long-term effects of diesel following acute exposure is mainly concerned with jet fuels [11, 31] and thus its relevance is uncertain due to the presence of chemical additives and different hydrocarbon profile. In general, single (acute) oral, dermal and ocular exposures do not appear to result in persistent effects.DIESEL – TOXICOLOGICAL OVERVIEW



## Health Effects of Chroni c / Repeated Exposure

Human Data

General toxicity

Under normal industrial or domestic use, dermal contamination is the most likely exposure scenario. Chronic or repeat exposure to diesel may result in dermatitis although there is some evidence to suggest that hyperkeratosis may be a common feature of regular contact with diesel [8].

Inhalation

There are currently no unequivocal studies to relate chronic or repeated diesel exposures to long-term pulmonary dysfunction (other than that associated with aspiration of contaminated water or vomit). There is limited evidence to suggest that chronic exposure to long-chain hydrocarbon mixtures may be associated with a tightness of chest and breathing difficulties, although a review of the duration and extent of exposure in such circumstances was not reported [31]. In one case, a lorry driver was exposed to (an unknown concentration of) diesel vapour over a ten day period. Signs and symptoms included abdominal cramps, nausea, vomiting, acute renal failure, anaemia and thrombocytopenia [32].

Ingestion

Chronic, oral exposure to diesel is unlikely to arise under normal circumstances and there is currently no data available on the chronic effects of diesel ingestion in humans.

Dermal / ocular exposure

There are no reports on the effects of chroni c ocular exposure to diesel in humans.

Acne and folliculitis have been reported in one subject who may have received chronic (occupational) exposure to diesel ([33] as reviewed in [8]). An investigation of Azerbaijan oil field workers identified hyperkeratosis as being associated with diesel exposure ([34] as reviewed in [8]).

Genotoxicity

There was evidence of increased chromosomal aberrations in a small cohort of drivers exposed to diesel ([35] as reviewed in [9]). However, the group size was small (6 smokers and 6 non-smokers) and the effects of exposure to other substances (such as diesel exhaust fumes) could not be discounted.DIESEL – TOXICOLOGICAL OVERVIEW

Carcinogenicity

In a multi-site, case-control study, there was evidence for an increased risk of prostate cancer and squamous cell carcinoma of the lung [36] but this effect could not be attributed to any particular chemical. The IARC have evaluated diesel fuels as being “not classifiable as to their carcinogenicity to humans (Group 3)” [9]: there is “inadequate evidence” to classify diesel as a human carcinogen and “limited evidenc e” for the carcinogenicity of diesel to experimental animals.

Reproductive and developmental toxicity

There is currently no information concerning the effects of diesel exposure on human reproduction and development. Exposure to diesel is not an indication for invasive prenatal diagnostic tests or termination of pregnancy [37].



### Animal and In-Vitro Data

General toxicity

A number of studies have reported hyaline dr oplet nephropathy syndrome in rats; this pathological response is not considered to be relevant to humans [8].

Inhalation

In one study, mice were exposed to diesel vapour at concentrations of 65, 135 and 204 mg

m -3 , 8 hours a day for 5 days (equating to a daily Ct of 31, 65 and 98 g min m -3 , respectively) [18]. Three of ten animals died in the highest dose group. There were no general effects noted in the lowest dose group.

Following exposure to diesel vapour ( ≤ 6 mg L -1 ; ≤ 6h duration; ≤ 3 week -1 ; ≤ 9 exposures), the primary signs of toxicity in rabbits were observed in the lung. Such effects included an increase in leukocytes in bronchial lavage (BAL) fluid and (non-dose dependent) changes in lung function parameters ([38] as reviewed by [8]).

No substantial signs of toxicity were observed in rats exposed to diesel aerosol ( ≤ 1.5 mg L -1 ; 4h per day; 2 week -1 ; 13 weeks): other signs deemed to be indicative of slight toxicity (including decreased weight and increase in BAL macrophages) were described as “generally reversible” following an eight week recovery period ([39] as reviewed by [8]).

Ingestion

There were no available reports on the chronic oral toxicity of diesel in animals.DIESEL – TOXICOLOGICAL OVERVIEW

Dermal / ocular exposure

Exposure of rabbits to diesel (4 or 8 ml kg -1 ; 24h day -1 ; 5 days week -1 ) for 14 days resulted indose-dependent dermal irritation and anorexia, leading to cachexia and death in the highestdose group [29].

Genotoxicity

Diesel was reported as being negative in the Ames Salmonella assay [40]. (This was interpreted as diesel being “weakly mutagenic” by the IARC [9]). In the same study, diesel was determined to be non-mutagenic in the L5178Y (TK +/- and TK -/- strains) mouse lymphoma assay. Dimethyl sulphoxide extracts of diesel (containing aromatic or aliphatic fractions) did not induce mutations in S. typhimurium TA100 ([41] as reviewed by [9]). No effect was observed on the frequency of dominant lethal mutations in mice (CD-1) exposed to diesel ( ≤ 400 ppm; 6 h day -1 ; 5 days week -1 ) for a total of 8 weeks ([8, 42] as reviewed by [8]).

In-vivo bone marrow clastogenicity studies showed a clear increase in chromosome aberrations only at very high dose levels (6 ml kg -1 body weight) [41]. No details of the type of aberration were provided and no definitive conclusions can be drawn.

The available data indicate that diesel does not have any mutagenic potential.

Carcinogenicity

It is generally considered that most middle-distillate fuels (e.g. kerosene, petrol and diesel) are non-genotoxic carcinogens [43-46].

In the most recent study of tumorigenic potential, rats were administered diesel by oral gavage (in olive oil) four times per week for 104 weeks [47]. The authors surmised that there was a non-dose dependent increase in the incidence of total malignant tumours (which may be of limited relevance) and an increase in uterus-vaginal malignant tumours (which was described as dose related). No further details are available.

Reproductive and developmental toxicity

No teratogenic (developmental) effects were observed in rats subject to inhalation of diesel vapour between gestational days 6 and 15 (6h day -1 ; 100 & 400 ppm) ([48] as reviewed in [9]).DIESEL – TOXICOLOGICAL OVERVIEW



## References

[1] Owen, K. and Coley, T. (1995). Automotive fuels reference book. In. ed. Society of Automotive Engineers, Inc. Warrendale, PA.

[2] BS EN 590:2004. Automotive fuels - Diesel - requirements and test methods. (2004).

[3] International Programme on Chemical Safety (IPCS) (1982). Environmental Health Criteria 20. Selected petroleum products. World Health Organisation. Geneva.

[4] Risher, J. F. and Rhodes, S. W. (1995). Toxicological profiles for fuel oils. US Department of Health and Human Sciences.

[5] Li, F. K., Yip, P. S., Chan, K. W., Chan, T. M. and Lai, K. N. (1999). Acute renal failure after immersion in seawater polluted by diesel oil. Am J Kidney Dis 34 , E26.

[6] Barrientos, A., Ortuno, M. T., Morales, J. M., Tello, F. M. and Rodicio, J. L. (1977). Acute renal failure after use of diesel fuel as shampoo. Arch Intern Med 137 , 1217.

[7] CONCAWE (1996). Gas oils (diesel fuels / heating oils). Report Number 95/107.

[8] International Programme on Chemical Safety (IPCS) (1996). Environmental Health Criteria 171. Diesel fuel and exhaust. World Health Organisation. Geneva.

[9] International Agency for the Research on Cancer (IARC) (1989). Occupational exposures in petroleum refining: Crude oil and major petroleum fuels. IARC Monographs on the evaluation of carcinogenic risks to humans. Lyon.

[10] Periago, J. F. and Prado, C. (2005). Evolution of occupational exposure to

environmental levels of aromatic hydrocarbons in service stations. Ann Occup Hyg

49 , 233-40.

[11] Ritchie, G. D., Still, K. R., Alexander, W. K., Nordholm, A. F., Wilson, C. L., Rossi, J., 3rd and Mattie, D. R. (2001). A review of the neurotoxicity risk of selected hydrocarbon fuels. J Toxicol Environ Health B Crit Rev 4 , 223-312.

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M.L. Kane. Princeton Scientific Publishers.

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Pediatrics 54 , 351-7.

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isothiazolinones in diesel oil. Contact Dermatitis 34 , 64-5.

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to common solvents. Contact Dermatitis 33 , 359-60.

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[30] Starek, A., L., F., Cembala, D. and Lepiarz, Q. (1975). Porownawcze badania nad toksycznoscia niektorych dielektrykow pochodnych ropy naftowej stosowanych w obrobce elektroerozyjnej. 1. Ocena ogolnej ostrej i podostrej toksycznosci. Medycyna Pracy 26 , 219-230.

[31] Ritchie, G., Still, K., Rossi, J., 3rd, Bekkedal, M., Bobb, A. and Arfsten, D. (2003). Biological and health effects of exposure to kerosene-based jet fuels and performance additives. J Toxicol Environ Health B Crit Rev 6 , 357-451.DIESEL – TOXICOLOGICAL OVERVIEW

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Dermatitis 18 , 120-1.

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Health 8 , 209-21.

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[39] Lock, S., Dalbey, W., Schmoyer, R. and Griesemer, R. (1984). Inhalation toxicity of Diesel-fuel obscurant in Sprague-Dawley rats. Chemical characterisation and toxicological evaluation of airborne mixtures. Final report, Phase 3, subchronic exposures. Oak Ridge National Laboratory.

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[41] Henderson, T. R., Li, A. P., Royer, R. E. and Clark, C. R. (1981). Increased cytotoxicity and mutagenicity of diesel fuel after reaction with NO2. Environ Mutagen

3 , 211-220.

[42] API (1981). Mutagenicity evaluation of diesel fuel in the mouse dominant lethal assay, final report. Amercian Petroleum Institute. Washington.

[43] McKee, R. H. and Plutnick, R. T. (1989). Carcinogenic potential of gasoline and diesel engine oils. Fundam Appl Toxicol 13 , 545-53.

[44] McKee, R. H., Plutnick, R. T. and Przygoda, R. T. (1989). The carcinogenic initiating and promoting properties of a lightly refined paraffinic oil. Fundam Appl Toxicol 12

, 748-56.

[45] Ingram, A. J., King, D. J., Grasso, P. and Sharratt, M. (1993). The early changes in mouse skin following topical application of a range of middle distillate oil products. J Appl Toxicol 13 , 247-57.

[46] Nessel, C. S. (1999). A comprehensive evaluation of the carcinogenic potential of

middle distillate fuels. Drug Chem Toxicol 22 , 165-80.DIESEL – TOXICOLOGICAL OVERVIEW

[47] Maltoni, C., Ciliberti, A., Pinto, C., Soffritti, M., Belpoggi, F. and Menarini, L. (1997). Results of long-term experimental carcinogenicity studies of the effects of gasoline, correlated fuels, and major gasoline aromatics on rats. Ann N Y Acad Sci 837 , 15-52.

[48] Schreiner, C. (1984). Petroleum and petroleum products: a brief review of studies to evaluate reproductive effects. In ' Advances in modern environmental toxicology. ' Volume 3: Assessment of reproductive and teratogenic hazards. Page 29-45. ed. M.S. Christian, W.M. Galbraith, P. Voytek and M.A. Mehlman. Princeton Scientific

Publishers. Princeton.DIESEL – TOXICOLOGICAL OVERVIEWAnnex I: Categories of Diesel Additives.CategoryConcentrationRangeExample(s)NotesAntioxidants9 – 25 ppmHinderedphenols (e.g. 2,4-dimethyl-6-tertbutylphenol).Prevent “gum-forming” reactionsStabilisers25 - 200 ppmPolymethacrylate, polyisobutanePrevent sediment formation if diesel product is preparedfrom craked components.Metal deactivators~10 ppmN,N’-disalicylidene-1,2-propanediamineChelate metal ionsCetane improvers200 – 800 ppm2-ethyl hexyl nitrateDecrease time between injection of ignition incombustion chamber.Combustion improvers0.2% v/vHistorically include barium, manganese andcopper.Catalytic effect on combustion. No longer in commonuse.Flow improvers500 ppmEthylene acetate / vinyl acetate polymersDetergents100 - 200Amines, amides, imidazolinesPrevent “gummy deposits”.Corrosion inhibitors5 ppmSurfactants based on esters or amine salts ofalkenyl succinic acids, alkyl orthophosphoricacids an014d aryl sulphonic acids.Primarily to protect pipelines during transport.Antistatic additives (StaticDisplacement Additives)1 – 5 ppmToluene, alkyl benzene sulphonate, mono anddi-alkyl salicylic and dodecyl sulphosuccinicacid (Cr and Ca salts).Added to prevent build-up of charge during bulk transferunder fast pumping rates.Dehazers and demulsifiers5 – 20 ppmQuaternary ammonium salts.Added to storage tanks on an ad hoc basis to removewater contamination.Lubricity additives0.03 w/w%Phosphate ester amides.Improve lubricity caused byhydrotreatment (to removesulphur).Anti-icersUp to 30 ppmAlcohols / glycols.Added to delivery tanks.Biocides200 ppmThiazine derivatives.Prevent bacterial spoilage onstorage in fuel tanks.Antifoamants10 – 20 ppmSilicone additives.Prevent foaming, allowing more more complete filling ofengine.Odour masks and odorants10 – 20 ppmNeutralise or mask smell.Drag reducers50 ppmHigh molecular weight, oil-soluble polymers.Reduce drag through pipelines to increase throughput.Table A1: summary of common additives used to improve burn, storage or transport characteristics of diesel [1].DIESEL – TOXICOLOGICAL OVERVIEW



## Annex II: UK Classification of Fuel Oils.

Category Crude Fraction Primary Application

A1 Automotive diesel fuel.

A2 Middle distillate Agricultural engine fuel.

C1 Paraffin Flue-less heating appliances.

C2 Kerosene Vaporising or atomising domestic heating appliances.

D Middle distillate Atomising burners for domestic, commercial or industrial applications.

E - H Residual

distillate Atomising burners for boilers or certain industrial engines which may require pre-treatment or additives.

Table A2: Classification of various grades of fuel oil according to crude distillate fraction (“crude fraction”) and application. Source: Annex A to BS 2869:1998.DIESEL – TOXICOLOGICAL OVERVIEW



## Annex III: UK Physicochemical Standards for Diesel

Property Minimum Maximum

Cetane No

. 51 - Density at 15 °C (kg m -3 ) 820 845 Viscosity at 40 °C (mm 2 s -1 ) 2.0 4.5 Flash point (°C) > 55 - Polycyclic aromatic hydrocarbons (% w/w)
- 11 Sulphur content (mg kg -1 )
- 50 Water content (mg kg -1 )
- 200 Ash content (% w/w)
- 0.01 Fatty acid methyl ester content (% v/v)
- 5

Table A3: Summary of standard physicochemical properties of diesel (BS EN 560:2004).

This document will be reviewed not later than 3 years or sooner if substantive evidence

becomes available.**S UBSTANCE**  **P ROFILES**  RUNNING



### Diesel Exhaust Particulates*
Reasonably anticipated to be a human carcinogen

First Listed in the Ninth Report on Carcinogens (2000)

Carcinogenicity
Exposure to diesel exhaust particulates is reasonably anticipated to be a human carcinogen, based on limited evidence of carcinogenicity from studies in humans, which indicates elevated lung cancer rates in occupational groups exposed to diesel exhaust (IARC 1989, Cohen and Higgens 1995, Bhatia et al. 1998) and supporting animal and mechanistic studies. An increased risk of lung cancer is found in the majority of human studies. The overall relative risk is approximately 1.3, and higher risks are found in more heavily exposed subgroups in some studies. The increased risk is not readily explained by confounding by either smoking or asbestos exposure. However, the increased risk cannot always be clearly ascribed to diesel exhaust exposure. Although some studies employed semiquantitative estimates of diesel exhaust exposure (Steenland et al. 1998), most studies used inadequate measures of exposure. Studies of the carcinogenicity of diesel exhaust particulates in animals have shown a consistent lung tumor response in rats but not in the mouse or hamster. The response in rats appears to be due to the particulate component of exhaust, as the filtered vapor phase of exhaust has been shown not to be tumorigenic. Solvent extracts of diesel exhaust particles are carcinogenic when applied to the skin or administered by intratracheal instillation or intrapulmonary implantation to rats, mice, or hamsters.
Additional Information Relevant to Carcinogenicity

Diesel exhaust is a complex mixture of combustion products of diesel fuel, with the exact composition depending on the type of engine, the speed and load at which it is run, and the composition of the fuel used. Diesel exhaust contains identified mutagens and carcinogens both in the vapor phase and associated with respirable particles. Diesel exhaust particles are considered likely to account for the human lung cancer findings because they are almost all of a size small enough to penetrate to the alveolar region. Mutagenic and carcinogenic chemicals, including polyaromatic hydrocarbons and nitroarenes, have been extracted from these particles with organic solvents, or with a lipid component of mammalian lung surfactant. While diesel particulate exposures produce lung cancer in rats, the relevance of this result in predicting the human response has been questioned. Diesel exhaust particulate exposure produces a spectrum of inflammatory and neoplastic pulmonary responses in the rat that are characteristic of responses also seen with other inhaled particles of varying toxicity. These responses are apparently little influenced by the chemical constituents of the particles. Although the precise bioavailability of chemical mutagens and carcinogens from inhaled diesel particulates is not known, DNA adducts have been found in the lung of rats exposed to diesel exhaust particulates. Similarly, more lymphocyte-DNA adducts were found in groups occupationally exposed to diesel exhaust than in groups with lower or ambient exposures. However, diesel exhaust exposure was not quantified in these studies, and exposure to used motor oil may have contributed to the adducts observed in one study.

Properties

Diesel exhaust is a complex mixture of combustion products of diesel fuel, with the exact composition dependent upon the type of engine, operating conditions, lubricating oil, additives, emission control system, and the composition of the fuel used (Ullman 1989, Obert 1973). Diesel engines are typically separated according to their service requirements, light-duty or heavy-duty. The operating conditions for light-duty and heavy-duty diesel engines differ in terms of engine speed, expected load, fuel composition, and engine emission controls. Typically light-duty vehicles such as automobiles and light trucks operate at higher speeds than heavy-duty vehicles such as trucks. The total particulate emission concentration from light-duty diesel engines is much smaller than from heavy-duty diesel engines. In general, newer heavy-duty trucks emit diesel particulates at a rate 20 times greater than catalyst-equipped gasoline-fueled vehicles (WHO 1996). However, depending on operating conditions, fuel composition, and engine control technology, light-duty diesel engines and heavy-duty diesel engines can emit 50 to 80 times and 100 to 200 times, respectively, more particulate mass than typical catalytically equipped gasoline engines (McClellan 1986). The particle size distribution of diesel exhaust is bi-modal with a nuclei mode (0.0075 to 0.042 μm in diameter) and an accumulation mode (0.042 to 1.0 μm in diameter) (Baumgard and Johnson 1996), most of which occur in aerodynamic diameters ranging from 0.1 to 0.25 μm in diameter (Groblicki and Begeman 1979, Dolan et al. 1980, NRC 1982, Williams 1982). Approximately 98% of the particles emitted from diesel engines are less than 10 microns in diameter, 94% less than 2.5 microns in diameter, and 92% less than 1.0 microns in diameter (ARB 1997). Engines running under low load typically produce fewer particles with a higher proportion of organic compounds associated with the available particle mass. Conversely, engines under high load typically produce more particulate matter with a lower proportion of organic compounds associated with available particles. Kishi et al. (1992) found that exhaust gas temperatures affect particle composition. Low exhaust gas temperatures produce particulate matter with more adsorbed soluble organics than particulate matter produced in a high exhaust gas temperature environment. The emissions consist of a nonpolar fraction (57%), a moderately polar fraction (9%), and a polar fraction (32%) (Schuetzle 1983,
Schuetzle et al. 1985), with the remainder unrecoverable. Diesel engines operate with excess air (~25-30 parts air to 1 part fuel) (Lassiter and Milby 1978). The gas phase fraction is composed primarily of typical combustion gases such as nitrogen, oxygen, carbon dioxide, and water vapor. As a result of incomplete combustion, the gaseous fraction also contains pollutants such as carbon monoxide, sulfur oxides, nitrogen oxides, volatile hydrocarbons, and low molecular weight polyaromatic hydrocarbons (PAHs) and their derivatives. The inorganic fraction of the particulate phase of diesel fuel combustion emissions primarily consists of small elemental carbon particles ranging from 0.01 to 0.08 μm in diameter. The organic and elemental carbon accounts for approximately 80% of the total particulate matter mass. The remaining 20% is composed of sulfate (mainly sulfuric acid) (Pierson and Brachaczek 1983) and some inorganic additives and components of fuel and motor oil. In general, the organic compounds identified in diesel exhaust emissions contain hydrocarbons, hydrocarbon derivatives, PAHs, PAH derivatives, multifunctional derivatives of PAHs, heterocyclic compounds, heterocyclic derivatives, and multifunctional derivatives of heterocyclic compounds (Schuetzle 1988). The organic fractions consist of soluble organic compounds such as aldehydes, alkanes, alkenes, and high molecular weight PAHs and PAH-derivatives. Because of their high surface area, diesel exhaust particulates are capable of adsorbing relatively large amounts of organic material. The adsorbed elements come from unburned fuel, lubricating oil, and pyrosynthesis during fuel combustion. A variety of mutagens and carcinogens such as PAH and nitro-PAH (NRC 1982, Tokiwa and Ohnishi 1986, WHO 1996) are adsorbed by the particulates. There is sufficient evidence for the carcinogenicity for 15 PAHs (a number of these PAHs are found in diesel exhaust particulate emissions) in experimental animals. The nitroarenes (five listed) meet the established criteria for listing as reasonably anticipated to be a human

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**LEVENTH E**  **DITION** carcinogen based on carcinogenicity experiments with laboratory animals. The organic extractable fraction of diesel exhaust particulates is typically in the 20% to 30% range but it may be as high as 90% (Williams et al. 1989), depending upon vehicle type and operating conditions. In general, incomplete combustion in diesel engines operating under low load conditions produces relatively low particle concentrations and a higher proportion of organic-associated particles (Dutcher et al. 1984).

Use

No known uses of diesel exhaust particulates exist.

Production

Internal combustion engines have been used in cars, trucks, locomotives, and other motorized machinery for approximately 100 years (IARC 1989). The combustion of diesel fuel in a compression ignition engine produces diesel exhaust. Engine exhaust contains thousands of gaseous and particulate substances. There are three major groups of diesel exhaust sources: mobile sources (on-road vehicles and other mobile sources), stationary area sources (oil and gas production facilities, stationary engines, repair yards, shipyards etc.), and stationary point sources (chemical manufacturing, electric utilities, etc.). The composition and quantity of the emissions from an engine depend mainly on the type and condition of the engine, fuel composition and additives, operating conditions, and emission control devices.

Exposure

Various employee groups have been studied to determine their occupational exposures to diesel exhaust particulates. They include railroad workers, mine workers (who use diesel-powered equipment), bus garage workers, trucking company workers, fork-lift truck operators, firefighters, lumberjacks, toll-booth and parking garage attendants, and many professions servicing or handling automobiles (car mechanics, professional drivers, etc. ). The National Institute for Occupational Safety and Health (NIOSH) has estimated that approximately 1.35 million workers are occupationally exposed to diesel exhaust particulates in approximately 80,000 workplaces in the United States (MMWR 1989). Railroad workers’ potential for exposure has increased since 1959, when almost all the U.S. railroad system (95%) was converted to diesel engines. Varying degrees of exposure to diesel exhaust particulates (from 17 μg/m 3 for clerks to 134 μg/m 3 for locomotive shop workers) has been reported based upon job groups (Woskie et al. 1988). Diesel engines have been, and continue to be, commonly used in U.S. mines since their first introduction in the early 1950s. Exposure occurs from activities that use diesel-fueled heavy machinery, such as blasting. Holland (1978) conducted an exposure study in 24 U.S. coal mines and showed that, while certain PAHs expected from diesel exhaust particulates were found (anthracene and phenanthrene), other PAHs (benz[ a ]anthracene, benz[ a ]pyrene, benz[ e ]pyrene, chrysene, and pyrene) were not found in measurable quantities. Cornwell (1982) found other PAHs not found in Holland’s study in diesel emissions from a molybdenum mine in Colorado. This mine was equipped with drills and various load haul-dumps. Bus repair facilities were studied to determine diesel exhaust emissions (Apol 1983). The highest exposure levels were observed when buses were started at peak times of dispatch and return. Pryor (1983) studied area levels of diesel exhaust particulates at a bus garage. Elevated levels of diesel exhaust emissions were observed during peak hours of bus activity. Levels rapidly returned to normal 10 to 15 minutes after the passing of peak times. Using elemental carbon,
Zaebst et al. (1991) found an effective way of determining truck drivers’ exposure to diesel exhaust particulates. Temperature was an important factor with higher exposures occurring at higher temperatures. This study showed no discernible difference between the exposure levels of truckers (3.8 μg/m 3 ) and highway background concentrations (2.5 μg/m 3 ). These results indicate that the highway environment, rather than the truck itself, is the cause of the truck driver’s exposure (Zaebst et al. 1991). Firefighters in New York, Boston, and Los Angeles were studied to determine exposure to diesel exhaust particulates (Froines et al. 1987). Total exposure to airborne particles was measured using personal air samplers. Approximately 86% of the study population were nonsmokers. Smokers were exposed to higher average airborne particle concentrations than were nonsmokers. Sampling was performed only when firefighters were in the fire stations. For the three cities, total airborne particulate exposure had a time-weighted average (TWA) ranging from below 100 μg/m 3 to 480 μg/m 3 . An average particulate exposure of 300 μg/m 3 was measured in Boston and New York. After adjustment for background levels and smoking (75 μg/m 3 ), firefighters in these two cities were exposed to a total diesel exhaust particulates level of 225 μg/m 3 . Los Angeles had the highest exposure levels of the three cities. For a “worst-case” scenario, the mean concentration levels were as high as 748 μg/m 3 . The authors noted that these were busy fire stations located in large metropolitan areas. Other factors such as smoking, building design, age and maintenance of vehicles, activities of the firefighters, and timing of runs also affected results. Three studies reviewed by the IARC (1989) found that toll-booth workers had elevated levels of exposure to carbon monoxide (although this was decreased with ventilation systems) and diesel exhaust particulates. carbon monoxide exposure also was elevated among border-station and motor vehicle inspectors and parking garage attendants (IARC 1989). In many of these studies, however, it was difficult to differentiate between gasoline exhaust and diesel exhaust. Numerous studies have combined the two types of exhausts together. Therefore, exact determinations of diesel exhaust particulates exposure is difficult in these cases.

Regulations

EPA
Clean Air Act

Control of Emissions of Hazardous Air Pollutants from Mobile Sources: Listed as a

Mobile Source Air Toxic for which regulations are to be developed

Guidelines

NIOSH Diesel exhaust listed as a potential occupational carcinogen

*No separate CAS registry number assigned to diesel exhaust particulates.

R EFERENCES

Apol, A. G. 1983. Health Hazard Evaulation, Regional Transportation District, Denver CO. HETA-82-137- 1264. Cincinnati, OH: National Institute for Occupational Safety and Health. ARB. 1997. Emission Inventory, 1995. Air Resource Board, Technical Support Division. Baumgard, K. J. and J. H. Johnson. 1996. The Effect of Fuel and Engine Design on Diesel Exhaust Particle Size Distributions. SAE Technical Paper Series, #960131. Bhatia, R., P. Lopipero and A. H. Smith. 1998. Diesel exhaust exposure and lung cancer. Epidemiology 9(1): 84-91. Cohen, A. J. and M. W. P. Higgins. 1995. Diesel Exhaust. A Critical Analysis of Emissions, Exposure, and

Health Effects. Health Effects Institute. Cornwell, R. J. 1982. Health Hazard Evaluation Determination: Climax Molybdenum Company, Climax, CO. Report No. MHETA-81-108-9004, PB84-14850 1. Morgantown, WV.
Dolan, D. F., D. B. Kittelson and D. Y. H. Pui. 1980. Diesel Exhaust Particle Size Distribution Measurement Techniques. SAE Technical paper # 870254.Dutcher, J. S., J. D. Sun, J. A. Lopez, I. Wolf, R. K. Wolff and R. O. McClellan. 1984. Generation and characterization of radiolabeled diesel exhaust. Am Ind Hyg Assoc J 45(7): 491-8. Froines, J. R., W. C. Hinds, R. M. Duffy, E. J. Lafuente and W. C. Liu. 1987. Exposure of firefighters to diesel emissions in fire stations. Am Ind Hyg Assoc J 48(3): 202-7. Groblicki, P. J. and C. R. Begeman. 1979. Particle size variation in diesel car exhaust. SAE Technical paper #790421. Society of Automotive Engineers. Holland, W. D. 1978. Determination of Breathing Zone Concentration of Contaminants from Emission from Diesel Powered Vehicles in Underground Mines. BuMines OFR 24-80; U.S. NTIS Pb80-150776. Washington, D.C.: U.S. Department of the Interior, Bureau of Mines. IARC. 1989. Diesel and Gasoline Engine Exhausts and Some Nitroarenes. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Humans, vol. 46. Lyon, France: International Agency for Research on Cancer. 458 pp. Kishi, Y., H. Tohno and M. Ara. 1992. Characteristics and Combustability of Particulate Matter. Reducing Emissions from Diesel Combustion. Warrendale, PA: Society of Automotive Engineers. p. 139-146.**S UBSTANCE**  **P ROFILES**  RUNNING

Lassiter, D. V. and T. H. Milby. 1978. Health Effects of Diesel Exhaust Emission: A Comprehensive Literature Review, Evaluation and Research Gaps Analysis. U.S. NTIS PB-282-795. Washington, D.C.: American Mining Congress. McClellan, R. O. 1986. 1985 Stokinger lecture. Health effects of diesel exhaust: a case study in risk assessment. Am Ind Hyg Assoc J 47(1): 1-13. MMWR. 1989. Publication of NIOSH Current Intelligence Bulletin on Carcinogenic Effects of Diesel Exhaust. Morbid Mort Weekly Report 38: 76-78. NCR. 1982. Diesel cars: benefits, risks, and public policy, final report of the Diesel Impacts Study Committee. Washington, D.C.: National Academy Press. Obert, E. F. 1973. Internal Combustion Engines and Air Pollution. Harper and Row.
Pierson, W. R. and W. W. Brachaczek. 1983. Particulate matter associated with vehicles on the road II.

Aerosol. Sci Tech 2: 1-40. Pryor, P. 1983. Trailways Bus System, Denver CO. Health Hazard Evaluation Report No. HETA 81-416-1334. Cincinnati, OH: National Institute of Occupational Safety and Health. Schuetzle, D. 1983. Sampling of vehicle emissions for Chemical Analysis and biological testing. Environ Health Perspect 47: 65-80.Schuetzle, D. 1988. Organic tracers for source apportionment of combustion emissions to ambient air particulates. In Proceedings of the Sixth Symposium on Environmental Analytical Chemisty and Source Apportionment in Ambient and Indoor Atmospheres. Schuetzle, D., T. E. Jensen and J. C. Ball. 1985. Polar PAH derivatives in extracts of particulates: Biological characterization and techniques for chemical analysis. Environ Int 11: 169-181. Steenland, K., J. Deddens and L. Stayner. 1998. Diesel exhaust and lung cancer in the trucking industry: exposure-response analyses and risk assessment. Am J Ind Med 34(3): 220-8. Tokiwa, H. and Y. Ohnishi. 1986. Mutagenicity and carcinogenicity of nitroarenes and their sources in the environment. Crit Rev Toxicol 17(1): 23-60. Ullman, T. L. 1989. Investigation of the Effects of Fuel Composition on Heavy Duty Diesel Engine Emissions. SAE Technical Paper No. 892072. Society of Automotive Engineers. WHO. 1996. Diesel Fuel and Exhaust Emissions. Geneva: World Health Organization.
Williams, D. J., J. W. Milne and D. B. K. Roberts, M.C. 1989. Particulate emission from "in use" motor

vehicles - II Diesel vehicles. Atmos Environ 23: 2647-2661. Williams, R. L. 1982. Diesel particulate emissions: composition, concentration, and control. Dev Toxicol

Environ Sci 10: 15-32. Woskie, S. R., T. J. Smith, S. K. Hammond, M. B. Schenker, E. Garshick and F. E. Speizer. 1988. Estimation of the diesel exhaust exposures of railroad workers: I. Current exposures. Am J Ind Med 13(3): 381-94. Zaebst, D. D., D. E. Clapp, L. M. Blade, D. A. Marlow, K. Steenland, R. W. Hornung, D. Scheutzle and J. Butler. 1991. Quantitative determination of trucking industry workers’ exposures to diesel exhaust particles. Am Ind Hyg Assoc J 52(12): 529-41.

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### Diesel fuel is widely used throughout our society. It powers trucks that deliver products to our communities, buses that carry us to school and work, agricultural equipment that plants and harvests our food, and backup generators that can provide electricity during emergencies. It is also used for many other applications. Diesel engines have historically been more versatile and cheaper to run than gasoline engines or other sources of power. Unfortunately, the exhaust from these engines contains substances that can pose a risk to human health.

In 1998, the California Environmental Protection Agency’s Office of Environmental Health Hazard Assessment (OEHHA) completed a comprehensive health assessment of diesel exhaust. This assessment formed the basis for a decision by the California Air Resources Board (ARB) to formally identify particles in diesel exhaust as a toxic air contaminant that may pose a threat to human health. The American Lung Association of California (ALAC) and its 15 local associations work to prevent lung disease and promote lung health. Since 1904, the American Lung Association has been fighting lung disease through education, community service, advocacy

and research.

This fact sheet by OEHHA and ALAC provides

information on health hazards associated with diesel

exhaust.



## What is diesel exhaust?

Diesel exhaust is produced when an engine burns diesel fuel. It is a complex mixture of thousands of gases and fine particles (commonly known as soot) that contains more than 40 toxic air contaminants. These include many known or suspected cancer-causing substances, such as benzene, arsenic and formaldehyde. It also contains other harmful pollutants, including nitrogen oxides (a component of urban smog).



## How are people exposed to diesel exhaust?

Diesel exhaust particles and gases are suspended in the air, so exposure to this pollutant occurs whenever a person breathes air that contains these substances. The prevalence of diesel-powered engines makes it almost impossible to avoid exposure to diesel exhaust or its byproducts, regardless of whether you live in a rural or urban setting. However, people living and working in urban and industrial areas are more likely to be exposed to this pollutant. Those spending time on or near roads and freeways, truck loading and unloading operations, operating diesel-powered machinery or 

# Diesel exhaust

contains more
than 40 toxic air

contaminants

### working near diesel equipment face exposure to higher levels of diesel exhaust and face higher health

risks.



## What are the health effects of diesel exhaust?

As we breathe, the toxic gases and small particles of diesel exhaust are drawn into the lungs. The microscopic particles in diesel exhaust are less than one-fifth the thickness of a human hair and are small enough to penetrate deep into the lungs, where they contribute to a range of health problems.

Diesel exhaust and many individual substances contained in it (including arsenic, benzene, formaldehyde and nickel) have the potential to contribute to mutations in cells that can lead to cancer. In fact, long-term exposure to diesel exhaust particles poses the highest cancer risk of any toxic air contaminant evaluated by OEHHA. ARB estimates that about 70 percent of the cancer risk that the average Californian faces from breathing toxic air pollutants stems from diesel exhaust particles.

In its comprehensive assessment of diesel exhaust, OEHHA analyzed more than 30 studies of people who worked around diesel equipment, including truck drivers, railroad workers and equipment operators. The studies showed these workers were more likely to develop lung cancer than workers who were not exposed to diesel emissions. These studies provide strong evidence that long-term occupational exposure to diesel exhaust increases the risk of lung cancer. Using information from OEHHA’s assessment, ARB estimates that diesel-particle levels measured in California’s air in 2000 could cause 540 “excess” cancers (beyond what would occur if there were no diesel particles in the air) in a population of 1 million people over a 70-year lifetime. Other researchers and scientific organizations, including the National Institute for Occupational Safety and Health, have calculated cancer risks from diesel exhaust that are similar to those developed by OEHHA and ARB.

Exposure to diesel exhaust can have immediate health effects. Diesel exhaust can irritate the eyes, nose, throat and lungs, and it can cause coughs, headaches, light-headedness and nausea. In studies with human volunteers, diesel exhaust particles made people with allergies more susceptible to the materials to which they are allergic, such as dust and pollen. Exposure to diesel exhaust also causes inflammation in the lungs, which may aggravate chronic respiratory symptoms and increase the frequency or intensity of asthma attacks.

Diesel engines are a major source of fine-particle pollution. The elderly and people with emphysema, asthma, and chronic heart and lung disease are especially sensitive to fine-particle pollution. Numerous studies have linked elevated particle levels in the air to increased hospital admissions, emergency room visits, asthma attacks and premature deaths among those suffering from respiratory problems. Because children’s lungs and respiratory systems are still developing, they are also more susceptible than healthy adults to fine particles. Exposure to fine particles is associated with increased frequency of childhood illnesses and can also reduce lung

function in children. 

# Diesel exhaust
increases the risk of

cancer...

... And it can cause coughs and aggravate asthma

# Diesel exhaust contributes to smog and fine-particle pollution Like all fuel-burning equipment, diesel engines produce nitrogen oxides, a common air pollutant in California. Nitrogen oxides can damage lung tissue, lower the body’s resistance to respiratory infection and worsen chronic lung diseases, such as asthma. They also react with other pollutants in the atmosphere to form ozone, a major component of smog.



## What is being done to reduce the health risks from diesel exhaust?

Improvements to diesel fuel and diesel engines have already reduced emissions of some of the pollutants associated with diesel exhaust. However, diesel exhaust is still one of the most widespread

and toxic substances in California’s air.

ARB’s Diesel Risk Reduction Plan, when fully implemented, will result in a 75 percent reduction in particle emissions from diesel equipment by 2010 (compared to 2000 levels), and an 85 percent reduction by 2020. The plan calls for the use of cleaner-burning diesel fuel, retrofitting of existing engines with particle-trapping filters, and the use in new diesel engines of advanced technologies that produce nearly 90 percent fewer particle emissions, as well as the use of alternative fuels.

The use of other fuels, such as natural gas, propane and electricity offer alternatives to diesel fuel. All of them produce fewer polluting emissions than current formulations of diesel fuel. As a result of ARB and local air-quality regulations, public transit agencies throughout California are using increasing numbers of passenger buses that operate with alternative fuels or retrofitted equipment.



## For further information

Office of Environmental Health Hazard Assessment

1001 I Street, P.O. Box 4010, Sacramento, CA 95812-4010 (916) 324-7572 www.oehha.ca.gov



### Air Resources Board

1001 I Street, Sacramento, CA 95814 (800) 363-7664 www.arb.ca.gov



### American Lung Association of California

921 11 th 

### Street, Suite 700, Sacramento, CA 95814 (916) 442-4446 For your local office, call (800) LUNG-USA www.californialung.org

The energy challenge facing California is real. Every Californian needs to take immediate action to reduce energy consumption. For a list of simple ways you can reduce demand and cut your energy costs, see OEHHA’s web site at www.oehha.ca.gov/public_info.html

.